Animals fed a high fat diet were limited to time restricted feeding during an eight hour period each day. The mice consumed the same number of calories as those allowed to eat all day and night yet they did not develop obesity or other health problems associated with the unrestricted mice. The time restricted feeding mice even developed improved motor coordination. The regimen also improved CREB, mTOR and AMPK anti-aging pathway functions and oscillations of the circadian clock and their target genes’ expression. These changes in catabolic and anabolic pathways altered liver metabolome, improved nutrient utilization and energy expenditure. The study demonstrated in mice that the time restricted feeding regimen is a non-pharmacological strategy against obesity and associated diseases.

Improvements were found in the time restricted feeding group in the following areas:

• Fatty acid metabolism, body weight and liver health
• Glucose metabolism and tolerance
• Overt rhythms and attenuated body weight gain
• CREB, mTOR and AMPK activities and in circadian oscillator
• Diurnal rhythms in metabolic regulators and the circadian oscillator
• Hepatic glucose metabolism
• Lipid homeostasis
• Bile acid production, adipose tissue homeostasis and inflammation alleviation

The published study can be viewed at Cell Metab. 2012 Jun 6; 15(6): 848?860

After I first learned about the massive number of people suffering from Vitamin D deficiency I went to my doctor and had a blood test called 25-hydroxyvitamin D. I expected that since I have a very healthy diet, take lots of supplements and exercise outdoors (with sunscreen) that my level would be high. It turned out that my blood showed a low level of Vitamin D. Our main source is sun exposure, yet it is a double edged sword since being exposed to the sun without sunscreen can cause skin damage, premature aging of the skin and other more serious problems. When wearing sunscreen your body can’t make much Vitamin D. I started taking 5000 IU/day of Vitamin D3 and after a few months I tested in the middle of the normal range. I have continued to take that much Vitamin D for years now and my yearly blood tests continue to be in the middle of the normal range. Everyone is different so the recommendation is to get tested and if you are low take at least 1000 IU of Vitamin D3/day or even as much as 5000 IU/day depending upon your blood test results and your doctors recommendations. Given the large amount of time that most people spend indoors combined with the use of sunscreen the RDA of 400 IU of Vitamin D is not enough for a massive number of people.

Following is a summary of the article “The Vitamin D Epidemic and its Health Consequences” that was published in The Journal of Nutrition.

“Vitamin D deficiency is now recognized as an epidemic in the United States. The major source of vitamin D for both children and adults is from sensible sun exposure. In the absence of sun exposure 1000 IU of cholecalciferol is required daily for both children and adults. Vitamin D deficiency causes poor mineralization of the collagen matrix in young children?s bones leading to growth retardation and bone deformities known as rickets. In adults, vitamin D deficiency induces secondary hyperparathyroidism, which causes a loss of matrix and minerals, thus increasing the risk of osteoporosis and fractures. In addition, the poor mineralization of newly laid down bone matrix in adult bone results in the painful bone disease of osteomalacia. Vitamin D deficiency causes muscle weakness, increasing the risk of falling and fractures. Vitamin D deficiency also has other serious consequences on overall health and well-being. There is mounting scientific evidence that implicates vitamin D deficiency with an increased risk of type I diabetes, multiple sclerosis, rheumatoid arthritis, hypertension, cardiovascular heart disease, and many common deadly cancers. Vigilance of one?s vitamin D status by the yearly measurement of 25-hydroxyvitamin D should be part of an annual physical examination. ”

“Vitamin D, known as the ?sunshine vitamin,? has been taken for granted and, until recently, little attention has been focused on its important role for adult bone health and for the prevention of many chronic diseases. It has been assumed that vitamin D deficiency is no longer a health issue in the United States and Europe. However, it is now recognized that everyone is at risk for vitamin D deficiency.”

The full article published in The Journal of Nutrition can be found here: https://jn.nutrition.org/content/135/11/2739S.full

In a study of more than 17,000 Canadians published in 2009 by Dr Peter Katzmarzyk and colleagues at the Pennington Biomedical Research Center they found links between time spent sitting and mortality. “Individuals who sat the most were roughly 50% more likely to die during the follow-up period than individuals who sat the least, even after controlling for age, smoking, and physical activity levels.”

Now new research suggests that taking short but frequent walks can counteract the harm caused by sitting for long periods of time.

The researchers found that even just a five-minute stroll can help.

“American adults sit for approximately eight hours a day,” study author Saurabh Thosar, now a postdoctoral researcher at Oregon Health & Science University, said in an Indiana University news release. “The impairment in endothelial function is significant after just one hour of sitting. It is interesting to see that light physical activity can help in preventing this impairment.”

According to background information from Indiana University, sitting for a prolonged period of time can cause blood to pool in the legs. This happens because muscles are not contracting and pumping blood to the heart as effectively. As a result, the ability of blood vessels to expand from increased blood flow can become impaired. Being sedentary is also linked to high cholesterol and a larger waistline, which increase the risk for heart and metabolic disease.

“There is plenty of epidemiological evidence linking sitting time to various chronic diseases and linking breaking sitting time to beneficial cardiovascular effects, but there is very little experimental evidence,” said Thosar, who was a doctoral candidate at IU’s School of Public Health-Bloomington when the study was conducted. “We have shown that prolonged sitting impairs endothelial function, which is an early marker of cardiovascular disease, and that breaking sitting time prevents the decline in that function.”

The researchers examined the effects of three hours of sitting on 11 healthy men who were not obese. The men, who ranged in age from 20 to 35 years old, participated in two trials.

First, the men sat for three hours without moving their legs. When the study began and once every hour afterwards, the function of their femoral artery was measured with a blood pressure cuff and ultrasound technology.

During the second trial, the men sat for three hours but also walked on a treadmill for five minutes after 30 minutes, 1.5 hours and 2.5 hours. The men walked at a slow pace of 2 miles per hour. The function of their femoral artery was again measured with a blood pressure cuff and ultrasound technology.

Overall, the researchers found, the ability of the arteries in the legs to expand was reduced by as much as 50 percent after just one hour of sitting. The men who walked for five minutes for each hour they spent sitting, however, had no reduction in the function of their arteries during the three-hour period.

The researchers concluded that the increased muscle activity and blood flow from the small amount of exercise offset the negative impacts of sitting.

By Mary Elizabeth Dallas in HealthDay News. The research was published Sept. 8 in the journal Medicine & Science in Sports & Exercise.

UCLA biologists have identified a gene that can slow the aging process throughout the entire body when activated remotely in key organ systems.

Working with fruit flies, the life scientists activated a gene called AMPK that is a key energy sensor in cells; it gets activated when cellular energy levels are low.

Increasing the amount of AMPK in fruit flies? intestines increased their lifespans by about 30 percent to roughly eight weeks from the typical six weeks and the flies stayed healthier longer as well.

Stem Cell 100^TM and Stem Cell 100+^TM both contain several compounds that activate AMPK. They also act on a number of additional anti-aging pathways which allowed us to double fruit fly lifespan as well as greatly increase their healthspan (the length of time they were healthy and active).

The research, published in the open-source journal Cell Reports, could have important implications for delaying aging and disease in humans, said David Walker, an associate professor of integrative biology and physiology at UCLA and senior author of the research.

?We have shown that when we activate the gene in the intestine or the nervous system, we see the aging process is slowed beyond the organ system in which the gene is activated,? Walker said.

Walker said that the findings are important because extending the healthy life of humans would presumably require protecting many of the body?s organ systems from the ravages of aging, but delivering anti-aging treatments to the brain or other key organs could prove technically difficult. The study suggests that activating AMPK in a more accessible organ such as the intestine, for example, could ultimately slow the aging process throughout the entire body, including the brain.

Humans have AMPK, but it is usually not activated at a high level, Walker said.

?The ultimate aim of our research is to promote healthy aging in people.?

The fruit fly, Drosophila melanogaster, is a good model for studying aging in humans because scientists have identified all of the fruit fly?s genes and know how to switch individual genes on and off. The biologists studied approximately 100,000 of them over the course of the study.

Lead author Matthew Ulgherait, who conducted the research in Walker?s laboratory as a doctoral student, focused on a cellular process called autophagy, which enables cells to degrade and discard old, damaged cellular components. By getting rid of that ?cellular garbage? before it damages cells, autophagy protects against aging, and AMPK has been shown previously to activate this process.

Ulgherait studied whether activating AMPK in the flies led to autophagy occurring at a greater rate than usual.

?A really interesting finding was when Matt activated AMPK in the nervous system, he saw evidence of increased levels of autophagy in not only the brain, but also in the intestine,? said Walker, a faculty member in the UCLA College. ?And vice versa: Activating AMPK in the intestine produced increased levels of autophagy in the brain and perhaps elsewhere, too.?

?Matt moved beyond correlation and established causality,? he said. ?He showed that the activation of autophagy was both necessary to see the anti-aging effects and sufficient; that he could bypass AMPK and directly target autophagy.?

In research published last year, Walker and his colleagues identified another gene, called parkin, which delayed the onset of aging and extended the healthy life span of fruit flies.

Source: UCLA

By 2050, the number of people over the age of 80 will triple globally, which could come at great cost to individuals and economies. In a commentary published July 24 in Nature, three experts call for moving forward with preclinical and clinical strategies for people that have been shown to delay aging in animals. In addition to promoting a healthy diet and regular exercise, these strategies include slowing the metabolic and molecular causes of human aging, such as the incremental accumulation of cellular damage that occurs over time.

Unfortunately, medicine focuses almost entirely on fighting chronic diseases in a piecemeal fashion as symptoms develop. Instead, more efforts should be directed to promoting interventions that have the potential to prevent multiple chronic diseases and extend healthy lifespans.

The researchers, at Washington University School of Medicine in St. Louis, Brescia University in Italy, the Buck Institute for Aging and Research and the Longevity Institute at the University of Southern California, write that unfortunately, economic incentives in biomedical research and health care reward treating disease more than promoting good health.

The problems of old age come as a package. More than 70% of people over 65 have two or more chronic conditions. Studies of diet, genes and drugs indicate that delaying one age-related disease probably staves off others. At least a dozen molecular pathways seem to set the pace of physiological ageing.

Researchers have tweaked these pathways to give rodents long and healthy lives. Restricting calorie intake in mice or introducing mutations in nutrient-sensing pathways can extend lifespans by as much as 50%. And these ‘Methuselah mice’ are more likely than controls to die without any apparent diseases. In other words, extending lifespan also seems to increase ‘healthspan’, the time lived without chronic age-related conditions.

Research has highlighted potential benefits from dietary restriction in extending healthy life span. People who eat significantly fewer calories, while still getting optimal nutrition, have ?younger,? more flexible hearts. They also have significantly lower blood pressure, much less inflammation in their bodies and their skeletal muscles function in ways similar to muscles in people who are significantly younger.

These insights have made hardly a dent in human medicine. Biomedicine takes on conditions one at a time. Rather, it should learn to stall incremental cellular damage and changes that eventually yield several infirmities.

The current tools for extending healthy life ? better diets and regular exercise ? are effective. But there is room for improvement, especially in personalizing treatments. Molecular insights from animals should be tested in humans to identify interventions to delay ageing and associated conditions. Together, preclinical and clinical researchers must develop meaningful endpoints for human trials.

Longevity pathways identified in model organisms seem to be conserved in humans and can be manipulated in similar ways. Genetic surveys of centenarians implicate hormonal and metabolic systems. Long-term calorie restriction in humans induces drastic metabolic and molecular changes that resemble those of younger people, notably in inflammatory and nutrient-sensing pathways. Mice engineered to have reduced signalling in these pathways live longer.

Several molecular pathways that increase longevity in animals are affected by approved and experimental drugs. The sirtuin proteins, involved in a similar range of cellular processes, are activated by high concentrations of naturally occurring compounds and extend lifespan in metabolically abnormal obese mice. A plethora of natural and synthetic molecules affect pathways that are shared by ageing and conditions related to ageing.

Diet has similar effects. The drugs rapamycin and metformin mimic changes observed in animals fed calorie and protein-restricted diets. And fasting triggers cellular responses that boost stress resistance, and reduce oxidative damage and inflammation. In rodents, fasting protects against diabetes, cancer, heart disease and neurodegeneration9. There are many anti-ageing interventions that could be considered for clinical trials.

Ignored opportunities

Scientists are not set up to capitalize on these leads to combat the looming ageing crisis. Clinicians do not realize how much is understood about the molecular mechanisms of ageing and its broad effects on diseases. Researchers of all stripes focus too much on easing or reversing the progression of diseases.

The problem is calcified by the funding gap. Budgets for ageing research are small compared to disease-centred research. The Division of Aging Biology in the US National Institute on Aging receives less than 1% of the National Institutes of Health’s budget even though it supports research into the mechanisms underlying most disabilities and chronic diseases. Most grants focus on diseases of specific systems. Most study sections are not set up to evaluate multidisciplinary research on healthspan. The situation is similar in Europe and Japan.

How should we test interventions that extend healthspan? Human data from dietary restriction and genetic-association studies of healthy ageing could help to channel the most promising pathways identified in preclinical studies. Animal studies should be designed to better mimic human ageing. For example, frailty indices are often used in human studies. Comparable indices should be developed for mice.

Suitable endpoints for human trials are needed. Animal work suggests many candidates as potential biomarkers, such as accumulation of molecular damage to DNA, proteins and lipids from oxidative stress. Publicly funded clinical trials could also collect crucial samples of blood, muscle and fat for molecular analysis.

Funding agencies should establish committees of translational scientists to review which markers of biological ageing are most consistent between animals and humans, and prioritize the most practical for further assessment. Chosen biomarkers could be evaluated in clinical studies over a broad age range of patients already being treated with drugs that increase lifespan in animal models. Assessments must also be developed for dietary or other interventions that do not involve drugs.

The most important change must be in mindset. Economic incentives in both biomedical research and health care reward treating diseases more than promoting health. The launch of a few anti-ageing biotech companies such as Calico, created last year by Google, is promising. But public money must be invested in extending healthy lifespan by slowing ageing. Otherwise we will founder in a demographic crisis of increased disability and escalating health-care costs.

A number of studies show that people who sleep approximately 6 1/2 – 7 hours each night live longer and have better cognitive function than those sleeping 8 hours or more.

Daniel F. Kripke, an Emeritus Professor of Psychiatry at the University of California San Diego, analyzed the data on 1.1 million people over a six year period who participated in a cancer study. Published in JAMA Psychiatry the study showed that people who reported they slept 6.5 – 7.4 hours had a lower mortality rate than those who slept for a shorter or longer length of time.

In another study, published in the journal Sleep Medicine in 2011, Dr. Kripke found further evidence that the optimal amount of sleep might be less than the traditional eight hours. The researchers recorded the sleep activity of about 450 elderly women using devices on their wrist for a week. Some 10 years later the researchers found that those who slept fewer than five hours or more than 6.5 hours had a higher mortality.

A study in the journal Frontiers in Human Neuroscience last year used data from users of the cognitive-training website Lumosity. Researchers looked at the self-reported sleeping habits of about 160,000 users who took spatial-memory and matching tests and about 127,000 users who took an arithmetic test. They found that cognitive performance increased as people got more sleep, reaching a peak at seven hours before starting to decline.

A study in the current issue of Journal of Clinical Sleep Medicine tracked five healthy adults who were placed in what the researchers called Stone-Age-like conditions in Germany for more than two months? without electricity, clocks, or running water. Participants fell asleep about two hours earlier and got on average 1.5 hours more sleep than was estimated in their normal lives, the study said. Their average amount of sleep per night was 7.2 hours.

We do not have to lose our independence and ability to live life in our 70’s or 80’s. Even at the age of 100 years old Fauja Singh completed a marathon.

The race ended just after Fauja Singh crossed the line in 3,851st place. By finishing then he would do what no man before him had ever done. Amid the bundled and cheering crowd in Toronto, underneath a distended but gracious sky, he would complete a marathon. And he would do so at 100 years old.

Was it pain he felt as he approached the end, just footsteps away from redefining the limits of human endurance? No, this wasn’t pain. Fauja knew pain. This wasn’t pain but exhaustion. And Fauja could handle exhaustion, because exhaustion foreshadowed euphoria. When Fauja got tired, it often meant a record would soon fall.

He’d already broken a few. Fastest to run a marathon (male, over age 90), fastest to run 5,000 meters (male, over age 100), fastest to run 3,000 meters (male, over age 100), and on and on they went. But those records didn’t roll off the tongue the way this one would. Oldest person to complete a marathon (male): Fauja Singh.

So Fauja ran in Toronto, arms swinging, yellow turban bobbing, chest-length Zeusian beard swaying in the wind. He was joined by other runners with roots in the Indian region of Punjab, their appearance in keeping with the traditions of their Sikh faith. Fauja trotted for the first three miles, until his coach encouraged him to slow to a jog. Speed was fleeting, the enemy of endurance. By mile 6, he’d downshifted to a toddle. After a break for a rubdown and some tea at mile 18, he settled into a walk.

The exhaustion took hold sometime around mile 20, but Fauja stayed upbeat about the remaining distance. Finally Fauja saw the only mile-marker that mattered: the finish line. What had been silence between footsteps was now music and cheers. The slog to the finish reminded Fauja of his wedding day, of the joy that awaited at the end of the long aisle. He waved to the crowd as he walked across the line, then lifted his arms and accepted a medal. He’d finished in 8 hours, 25 minutes. There were smiles and handshakes and photos with friends and strangers, then a rambling news conference for Fauja to reflect on his record.

Researchers at the University of California, Berkeley, have discovered that the hormone oxytocin plays a critical role in healthy muscle maintenance and repair. After a nine-day treatment of old mice, scientists found that the muscles of the group that had received oxytocin injections healed far better than those of a control group without oxytocin.
?The action of oxytocin was fast,? said Elabd a University of California Researcher. ?The repair of muscle in the old mice was at about 80 percent of what we saw in the young mice.?

A few other biochemical factors in blood have been connected to aging and disease in recent years, but oxytocin is the first anti-aging molecule identified that is approved by the Food and Drug Administration for clinical use in humans.

Oxytocin is a hormone associated with maternal nurturing, social attachments, childbirth and sex and is indispensable for healthy muscle maintenance and repair, and that in mice, it declines with age.

The new study published in the journal Nature Communications, presents oxytocin as the latest treatment target for age-related muscle wasting, or sarcopenia.

A few other biochemical factors in blood have been connected to aging and disease in recent years, but oxytocin is the first anti-aging molecule identified that is approved by the Food and Drug Administration for clinical use in humans, the researchers said. Pitocin, a synthetic form of oxytocin, is already used to help with labor and to control bleeding after childbirth. Clinical trials of an oxytocin nasal spray are also underway to alleviate symptoms associated with mental disorders such as autism, schizophrenia and dementia.

Oxytocin is sometimes referred to as the “trust hormone” because of its association with romance and friendship. It is released with a warm hug, a grasped hand or a loving gaze, and it increases libido. The hormone kicks into high gear during and after childbirth, helping new mothers bond with and breastfeed their new babies.

“This is the hormone that makes your heart melt when you see kittens, puppies and human babies,” said Conboy, who is also a member of the Berkeley Stem Cell Center and of the California Institute for Quantitative Biosciences (QB3). “There is an ongoing joke among my research team that we’re all happy, friendly and trusting because oxytocin permeates the lab.”

The researchers pointed out that while oxytocin is found in both young boys and girls, it is not yet known when levels of the hormone start to decline in humans, and what levels are necessary for maintaining healthy tissues.

Christian Elabd and Wendy Cousin, both senior scientists in Conboy’s lab, were co-lead authors on this study.

Previous research by Elabd found that administering oxytocin helped prevent the development of osteoporosis in mice that had their ovaries removed to mimic menopause.

The new study determined that in mice, blood levels of oxytocin declined with age. They also showed that there are fewer receptors for oxytocin in muscle stem cells in old versus young mice.

To tease out oxytocin’s role in muscle repair, the researchers injected the hormone under the skin of old mice for four days, and then for five days more after the muscles were injured. After the nine-day treatment, they found that the muscles of the mice that had received oxytocin injections healed far better than those of a control group of mice without oxytocin.

“The action of oxytocin was fast,” said Elabd. “The repair of muscle in the old mice was at about 80 percent of what we saw in the young mice.”

Interestingly, giving young mice an extra boost of oxytocin did not seem to cause a significant change in muscle regeneration.

“This is good because it demonstrates that extra oxytocin boosts aged tissue stem cells without making muscle stem cells divide uncontrollably,” Cousin added.

The researchers also found that blocking the effects of oxytocin in young mice rapidly compromised their ability to repair muscle, which resembled old tissue after an injury.

The researchers also studied mice whose gene for oxytocin was disabled, and compared them with a group of control mice. At a young age, there was no significant difference between the two groups in muscle mass or repair efficiency after an injury. It wasn’t until the mice with the disabled oxytocin gene reached adulthood that signs of premature aging began to appear.

“When disabling other types of genes associated with tissue repair, defects appear right away either during embryonic development, or early in life,” said Conboy. “To our knowledge, the oxytocin gene is the only one whose impact is seen later in life, suggesting that its role is closely linked to the aging process.”

Cousin noted that oxytocin could become a viable alternative to hormone replacement therapy as a way to combat the symptoms of both female and male aging, and for long-term health. Hormone therapy did not show improvements in agility or muscle regeneration ability, and it is no longer recommended for disease prevention because research has found that the therapy’s benefits did not outweigh its health risks.

In addition to healthy muscle, oxytocin is predicted to improve bone health, and it might be important in combating obesity.

Conboy said her lab plans to examine oxytocin’s role in extending a healthy life in animals, and in conserving its beneficial anti-aging effects in humans.

She noted that there is a growing circle of scientists who believe that aging is the underlying cause of a number of chronic diseases.

“If you target processes associated with aging, you may be tackling those diseases at the same time,” said Conboy. “Aging is a natural process, but I believe that we can meaningfully intervene with age-imposed organ degeneration, thereby slowing down the rate at which we become progressively unhealthy.”

The reduced ability to respond to stress is a major characteristic of aging. Indeed, aging itself is a stressful condition. Therefore, reducing chronic causes of stress can promote longevity. Some of the best protein protectors against stress and aging are the Heat Shock Proteins (HSPs). The protective HSPs are induced whenever your body is exposed to stressing agents such as:

1. Alcohol, which is one of the likely reasons that one drink per day helps prolong life
2. Elevated body temperature
3. Environmental toxins such as heavy metals or toxic chemicals
4. Oxidative stress, which may explain part of the reason that limited exercise is beneficial

Besides their effects on stress response, HSPs also have a protective role in disease and aging. For example, much research has shown that HSPs help with cardiovascular, metabolic, and neurological disorders.

At the recent AGE research conference (May 31 to June 2, 2014), new data on HSPs was presented by Kalie Kavanagh at Wake Forest University in North Carolina. Long lived Centenarians have better heat shock response and some may have gene variants of HSPs that are protective. HSP levels typically decline with age. Experiments in monkeys to raise their HSPs preserved insulin sensitivity, lowered blood pressure, and increased endurance.

The most interesting information to come out of the HSP talk was the potential to increase your own HSP levels. The HSPs can be stimulated by raising your body temperature slightly for 10 to 30 minutes using available methods: soaking in a hot tub at 104 degrees or sitting in a steam sauna bath, or participating in any exercise in which you build up a sweat for 5 minutes or more. These activities all lead to higher HSP levels, which can remain elevated and protective for 24 hours or more.

Have you ever wondered why aging occurs and how one might slow its progression? Aging expert Dr. Villeponteau describes dietary, exercise, and supplement routines that can add decades to your healthspan. Decoding Longevity condenses a wealth of practical information for those interesting in extending their health and longevity. Decoding Longevity also discusses the exponential increases in technology that will likely lead to greatly expanded longevity while maintaining health and indpendence in the next 20 to 40 years.

Decoding Longevity offers a full spectrum biological and genetic analysis of the aging process in layman’s language. Starting with an analysis of why life expectancy increased 57% in the 20th Century, it then focuses on recommended lifestyle choices that can significantly extend your healthspan and youthful fitness. The third part looks in some detail at the last 20 years of aging research, while the final section explores future developments that will provide powerful tools for extending healthspan and longevity in the next 20 to 40 years.

The Author: Dr. Bryant Villeponteau has 25 years of scientific leadership in aging research and some 60 scientific journal and patent publications. He has a Ph.D. in Biology from UCLA and was Assistant Professor of Biological Chemistry at the University of Michigan Medical School in the Institute of Gerontology. Dr. Villeponteau later led the research group at Geron Corporation, where he was the lead inventor in cloning human telomerase, thereby winning the Distinguished Inventor Award for the 2nd best US patent of 1997. Since 2008, Dr. Villeponteau has used genetics and machine learning technologies to develop antiaging supplements and drugs. He also cofounded Centagen, a Colorado stem cell company.

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